Aspirin's effect on macrophages beyond its chemopreventive role in inflammation and cancer.

IF 5.3 2区医学 Q2 IMMUNOLOGY

Inflammopharmacology Pub Date : 2025-09-24 DOI:10.1007/s10787-025-01945-1

Nese Unver

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引用次数: 0

Abstract

Aspirin's antineoplastic activities are primarily executed by irreversibly prohibiting COX-1 in platelets, hindering platelet activation and the subsequent release of compounds that promote tumor development and metastasis. Activated platelets may enhance cancer cells' metastatic potential via direct interaction and/or the release of soluble mediators by inducing COX-2 overexpression. Aspirin's chemopreventive effects may be mediated by COX-independent mechanisms, such as suppressing NF-kB and Wnt/β-catenin signaling. On the other hand, aspirin's effects on macrophages include inflammation resolution, cytokine regulation, and increased phagocytosis. Aspirin has a dual action mechanism, inhibiting macrophage-driven inflammation while simultaneously actively encouraging resolution by increasing phagocytic capacity and anti-inflammatory signaling. These effects occur via both dose-dependent and dose-independent routes and may differ between acute and chronic inflammatory conditions. Key factors, such as macrophage infiltration, immunophenotype, and polarization, are required to appropriately evaluate aspirin's effects and assess its role in the progress of inflammatory disorders and cancer.

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阿司匹林对巨噬细胞的作用超出了它在炎症和癌症中的化学预防作用。

阿司匹林的抗肿瘤活性主要是通过不可逆地抑制血小板中的COX-1，阻碍血小板活化和随后促进肿瘤发展和转移的化合物的释放来实现的。活化的血小板可能通过直接相互作用和/或通过诱导COX-2过表达释放可溶性介质来增强癌细胞的转移潜能。阿司匹林的化学预防作用可能是由cox非依赖性机制介导的，如抑制NF-kB和Wnt/β-catenin信号传导。另一方面，阿司匹林对巨噬细胞的影响包括炎症消退、细胞因子调节和吞噬作用增加。阿司匹林具有双重作用机制，一方面抑制巨噬细胞驱动的炎症，另一方面通过增加吞噬能力和抗炎信号积极促进炎症消退。这些作用通过剂量依赖性和剂量非依赖性途径发生，并且在急性和慢性炎症条件下可能有所不同。需要巨噬细胞浸润、免疫表型和极化等关键因素来适当评估阿司匹林的作用，并评估其在炎症性疾病和癌症进展中的作用。

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来源期刊

Inflammopharmacology IMMUNOLOGYTOXICOLOGY-TOXICOLOGY

CiteScore

8.00

自引率

3.40%

发文量

200

期刊介绍： Inflammopharmacology is the official publication of the Gastrointestinal Section of the International Union of Basic and Clinical Pharmacology (IUPHAR) and the Hungarian Experimental and Clinical Pharmacology Society (HECPS). Inflammopharmacology publishes papers on all aspects of inflammation and its pharmacological control emphasizing comparisons of (a) different inflammatory states, and (b) the actions, therapeutic efficacy and safety of drugs employed in the treatment of inflammatory conditions. The comparative aspects of the types of inflammatory conditions include gastrointestinal disease (e.g. ulcerative colitis, Crohn''s disease), parasitic diseases, toxicological manifestations of the effects of drugs and environmental agents, arthritic conditions, and inflammatory effects of injury or aging on skeletal muscle. The journal has seven main interest areas: -Drug-Disease Interactions - Conditional Pharmacology - i.e. where the condition (disease or stress state) influences the therapeutic response and side (adverse) effects from anti-inflammatory drugs. Mechanisms of drug-disease and drug disease interactions and the role of different stress states -Rheumatology - particular emphasis on methods of measurement of clinical response effects of new agents, adverse effects from anti-rheumatic drugs -Gastroenterology - with particular emphasis on animal and human models, mechanisms of mucosal inflammation and ulceration and effects of novel and established anti-ulcer, anti-inflammatory agents, or antiparasitic agents -Neuro-Inflammation and Pain - model systems, pharmacology of new analgesic agents and mechanisms of neuro-inflammation and pain -Novel drugs, natural products and nutraceuticals - and their effects on inflammatory processes, especially where there are indications of novel modes action compared with conventional drugs e.g. NSAIDs -Muscle-immune interactions during inflammation [...]